Spread of SARS-CoV within the infected mice. It will be of interest to evaluate the treatmentefficacy of camostat or nafamostat for SARS-CoV-2 infection, and various clinical studies happen to be out there for camostat (phase I/II NCT04321096; phase I/II NCT04435015; phase II NCT04353284; phase II NCT04374019; phase II NCT04470544; phase II/III NCT04455815; phase III NCT04355052; phase IV NCT04338906) and nafamostat (phase II/III SIRT6 Formulation NCT04352400; phase II/III NCT04418128; phase II/III NCT04473053).HTRA Targeting Virus replication Step Soon after the viral genome is uncoated from nucleocapsid, viral genome replication and protein translation happen. Positivesense RNA viruses, as an illustration, coronaviruses and flaviviruses, directly use the viral genome as a template for viral protein translation working with host machinery. Negative-sense RNA viruses like filoviruses and myxoviruses, must create positive-sense RNA by the virally encoded polymerase, after which protein translation is initiated. Retrovirus and HBV replication involve a single additional step, copying RNA to DNA by utilizing virally encoded reverse transcriptase. DNA viruses should use a host RNA polymerase to create RNA from the viral DNA genome for protein translation. Many viruses replicate in certain compartments, so-called replication organelles, inside the cytoplasm, involving the aberrant lipid-rich membrane rearrangement (de Wilde et al., 2018). Specifically, some flaviviruses or alphaviruses replicate on an architecture composed of single-membrane spherules (den Boon and Ahlquist, 2010); whilst coronaviruses or picornaviruses form double-membrane vesicles as replicase websites (de Wilde et al., 2013; van der Schaar et al., 2016). To facilitate viral genome amplification, various host proteins or connected pathways are needed to generate a favorable environment for virus production. These host proteins or pathways that interact with viral proteins are best host-targeting antivirals having a potential comprehensive antiviral efficacy. Statins (HMG-CoA Reductase Inhibitors) Statins are reversible inhibitors of 3-hydroxy-3-methylglutarylCoA (HMG-CoA) reductase, a rate-limiting enzyme involved in cholesterol biosynthesis. The statins are clinically authorized to decrease cholesterol levels to prevent major and secondary cardiovascular diseases. There are actually various forms of statins, which include lovastatin, αvβ3 Purity & Documentation atorvastatin, fluvastatin, pitavastatin, pravastatin, rosuvastatin, and simvastatin. Simvastatin is on the list on the WHO’s necessary medicines. Statins have already been reported to inhibit a panel of disparate viruses such as the viruses inside the loved ones Flaviviridae (HCV, DENV, and ZIKV) (Ye et al., 2003; Soto-Acosta et al., 2017; Espa et al., 2019), HIV (Amet et al., 2008), HBV (Okuyama-Dobashi et al., 2015), MV (Robinzon et al., 2009), EBOV (Shrivastava-Ranjan et al., 2018), RSV (Gower and Graham, 2001), EBV (Katano et al., 2004; Cohen, 2005), PRV (Desplanques et al., 2010), SFTSV (Urata et al., 2018), and parainfluenza (Bajimaya et al., 2017), because cholesterol biosynthesis is required for the replication of these viruses. Statins effectively inhibit flaviviral replication either in cell cultures or in animal models. Lovastatin impairs HCV RNA replication by blocking geranylgeranylation of a host protein necessary for HCV replication. Statins inhibit infectious ZIKVFrontiers in Pharmacology | www.frontiersin.orgMay 2021 | Volume 12 | ArticleLi and PengDrug Repurposing for Antiviral Find out.